Circ‐AKT3 aggravates renal ischaemia‐reperfusion injury via regulating miR‐144‐5p /Wnt/β‐catenin pathway and oxidative stress. Issue 6 (16th November 2020)

• Record Type: Journal Article
• Authors: Xu, Yong; Jiang, Wei; Zhong, Lili; Li, Hailun; Bai, Lin; Chen, Xiaoling; Lin, Yongtao; Zheng, Donghui
• Is Part Of: Journal of cellular and molecular medicine. Volume 26:Issue 6(2022)
• Page Start: 1766
• Page End: 1775
• Publication Date: 2020-11-16
• Subjects: circ‐AKT3 -- circRNA -- miR‐144‐5p -- oxidative stress -- renal ischaemia‐reperfusion injury -- Wnt/β‐catenin signal; Cytology; Medicine; Molecular Biology; Cytologie -- Périodiques; Médecine -- Périodiques; Biologie moléculaire -- Périodiques; Cytology -- Periodicals; Medicine -- Periodicals; Molecular biology -- Periodicals; 611.01805
• DOI: 10.1111/jcmm.16072
• Languages: English
• ISSNs: 1582-1838

Abstract

Abstract: Renal ischaemia‐reperfusion (RI/R) injury is one major pathological state of acute kidney injury (AKI) with a mortality rate ranking 50% to 80%. MiR‐144‐5p acts as a molecular trigger in various diseases. We presumed that miR‐144‐5p might be involved RI/R injury progression. We found that RI/R injury decreased miR‐144‐5p expression in rat models. MiR‐144‐5p downregulation promoted cell apoptosis rate and activated Wnt/β‐catenin signal in RI/R injury rats. By performing bioinformatic analysis, RIP, RNA pull‐down, luciferase reporter experiments, we found that circ‐AKT3 sponged to miR‐144‐5p and decreased its expression in RI/R injury rats. Moreover, we found that circ‐AKT3 promoted cell apoptosis rate and activated Wnt/β‐catenin signal, and miR‐144‐5p mimic reversed the promotive effect of circ‐AKT3 in rat models. We also found that circ‐AKT3 increased the oxidative stress level in rat models. In conclusion, our study suggests that the circAKT3 is involved RI/R injury progression through regulating miR‐144‐5p/Wnt/β‐catenin pathway and oxidative stress.